2016 ESC Guidelines for the

diagnosis and treatment of

acute and chronic heart failure
 Definition of heart failure
 HF is a clinical syndrome characterized by typical
symptoms (e.g. breathlessness, ankle swelling and fatigue)
that may be accompanied by signs (e.g. elevated jugular
venous pressure, pulmonary crackles and peripheral
oedema) caused by a structural and/or functional cardiac
abnormality, resulting in a reduced cardiac output and/ or
elevated intracardiac pressures at rest or during stress.
 Demonstration of an underlying cardiac cause is central to
the diagnosis of HF.
 This is usually a myocardial abnormality causing systolic and/or
diastolic ventricular dysfunction.
 However, abnormalities of the valves, pericardium, endocardium, heart
rhythm and conduction can also cause HF (and more than one
abnormality is often present).
 The main terminology used to describe HF is historical
and is based on measurement of the LVEF.
 HF comprises a wide range of patients, from those with
 normal LVEF [typically considered as ≥50%; HF with preserved
EF (HFpEF)]
 reduced LVEF [typically considered as <40%;HF with reduced EF
(HFrEF)] .
 Patients with an LVEF in the range of 40–49% represent a ‘grey
area’, which we now define as HFmrEF.
 a patient who has never exhibited the typical symptoms and/or signs of HF
and with a reduced LVEF is described as having asymptomatic LV systolic
dysfunction.
 Patients who have had HF for sometime are often said to have ‘chronic HF’.
 A treated patient with symptoms and signs that have remained generally
unchanged for at least 1 month is said to be ‘stable’.
 If chronic stable HF deteriorates, the patient may be described as
‘decompensated’ and this may happen suddenly or slowly, often leading to
hospital admission, an event of considerable prognostic importance.
 New-onset (‘de novo’) HF may also present acutely, for example, as a
consequence of acute myocardial infarction (AMI), or in a subacute (gradual)
fashion, for example, in patients with a dilated cardiomyopathy (DCM), who
often have symptoms for weeks or months before the diagnosis becomes clear.
 ‘Congestive HF’ is a term that is sometimes used, and may describe acute or
chronic HF with evidence of volume overload.
 ‘advanced HF’ is used to characterize patients with severe symptoms,
recurrent decompensation and severe cardiac dysfunction
 Epidemiology, aetiology and natural history of
heart failure

 The prevalence of HF depends on the definition

applied, but is approximately 1–2% of the adult
population in developed countries, rising to ≥10%
among people >70 years of age.
 The lifetime risk of HF at age 55 years is 33% for
men and 28% for women
 All-cause mortality is generally higher in HFrEF than
HFpEF.
 Symptoms and signs

 Symptoms are often non-specific and do not,

therefore, help discriminate between HF and other
problems.
 Symptoms and signs may be particularly difficult to
identify and interpret in obese individuals, in the
elderly and in patients with chronic lung disease.
 Younger patients with HF often have a different
aetiology, clinical presentation and outcome
compared with older patients.
Essential initial investigations: natriuretic peptides,
electrocardiogram and echocardiography
 The upper limit of normal in the non-acute setting for B-type natriuretic peptide (BNP)
is 35 pg/mL and for N-terminal pro-BNP (NT-proBNP) it is 125 pg/mL;
 in the acute setting, higher values should be used [BNP < 100 pg/mL, NT-proBNP <
300 pg/ mL and mid-regional pro A-type natriuretic peptide (MR-proANP) < 120
pmol/L].
 Therefore, the use of NPs is recommended for ruling-out HF, but not to establish the
diagnosis.
 AF, age and renal failure are the most important factors impeding the interpretation of
NP measurements. On the other hand, NP levels may be disproportionally low in obese
patients.
 An abnormal electrocardiogram (ECG) increases the likelihood of the diagnosis of HF,
but has low specificity. Some abnormalities on the ECG provide information on
aetiology (e.g. myocardial infarction), and findings on the ECG might provide
indications for therapy (e.g. anticoagulation for AF, pacing for bradycardia, CRT if
broadened QRS complex). HF is unlikely in patients presenting with a completely
normal ECG (sensitivity 89%). Therefore, the routine use of an ECG is mainly
recommended to rule out HF.
 Echocardiography is the most useful, widely available test in patients with suspected HF
to establish the diagnosis. It provides immediate information on chamber volumes,
ventricular systolic and diastolic function, wall thickness, valve function and pulmonary
hypertension. Other tests are generally required only if the diagnosis remains uncertain
(e.g. if echocardiographic images are suboptimal or an unusual cause of HF is
suspected)
Algorithm for the diagnosis of heart failure in the
non-acute setting

 For patients presenting with symptoms or signs for

the first time, non-urgently in primary care or in a
hospital outpatient clinic, the probability of HF
should first be evaluated based on the patient’s prior
clinical history, physical examination and resting
ECG. If at least one element is abnormal, plasma
NPs should be measured, if available, to identify
those who need echocardiography (an
echocardiogram is indicated if the NP level is above
the exclusion threshold or if circulating NP levels
cannot be assessed).
 Diagnosis of heart failure with preserved ejection
fraction
 The diagnosis of HFpEF remains challenging. LVEF is normal and signs and symptoms
for HF are often non-specific and do not discriminate well between HF and other
clinical conditions.
 The diagnosis of HFpEF requires the following conditions to be fulfilled:
 The presence of symptoms and/or signs of HF
 A ‘preserved’ EF (defined as LVEF ≥50% or 40–49% for HFmrEF)
 Elevated levels of NPs (BNP >35 pg/mL and/or NT-proBNP >125 pg/mL)
 Objective evidence of other cardiac functional and structural alterations underlying HF
 In case of uncertainty, a stress test or invasively measured elevated LV filling pressure may be needed to
confirm the diagnosis.
 Key structural alterations are a left atrial volume index (LAVI) >34 mL/m2 or a left
ventricular mass index (LVMI) ≥115 g/m2 for males and ≥95 g/m2 for females. Key
functional alterations are an E/e′ ≥13 and a mean e’septal and lateral wall <9 cm/s.
 A diastolic stress test can be performed with echocardiography, typically using a semi-
supine bicycle ergometer exercise protocol with assessment of LV (E/e′) and
pulmonary artery pressures (TRV), systolic dysfunction (longitudinal strain), stroke
volume and cardiac output changes with exercise.
 Alternatively,invasive haemodynamics at rest with assessment of filling pressures
[pulmonary capillary wedge pressure (PCWP) ≥15 mmHg or left ventricular end
diastolic pressure (LVEDP) ≥16 mmHg] followed by exercise haemodynamics if below
these thresholds, with assessment of changes in filling pressures, pulmonary artery
systolic pressure, stroke volume and cardiac output, can be performed
 Cardiac imaging and other diagnostic tests

 Cardiac imaging plays a central role in the diagnosis of

HF and inguiding treatment. Of several imaging
modalities available,
 echocardiography is the method of choice in patients with suspected
HF, for reasons of accuracy, availability (including portability), safety
and cost
 Chest X-ray
 Cardiac magnetic resonance
 Single-photon emission computed tomography and radionuclide
ventriculography
 Positron emission tomography
 Coronary angiography
 Cardiac computed tomography
 Genetic testing in heart failure
 Chest X-ray

 It is probably most useful in identifying an

alternative, pulmonary explanation for a patient’s
symptoms and signs, i.e. pulmonary malignancy and
interstitial pulmonary disease, although computed
tomography (CT) of the chest is currently the
standard of care.
 The chest X-ray may, however, show pulmonary
venous congestion or oedema in a patient with HF.
 It is important to note that significant LV
dysfunction may be present without cardiomegaly on
the chest X-ray.
 Congestive heart failure (CHF) is one of the most common
abnormalities evaluated by CXR. CHF may progress to pulmonary
venous hypertension and pulmonary edema with leakage of fluid
into the interstitium, alveoli and pleural space.
 The earliest CXR finding of CHF is cardiomegaly, detected as an
increased cardiothoracic ratio (>50%). In the pulmonary
vasculature of the normal chest, the lower zone pulmonary veins are
larger than the upper zone veins due to gravity. In a patient with
CHF, the pulmonary capillary wedge pressure rises to the 12-18
mmHg range and the upper zone veins dilate and are equal in size
or larger, termed cephalization. With increasing PCWP, (18-24 mm.
Hg.), interstitial edema occurs with the appearance of Kerley
lines. Increased PCWP above this level is alveolar edema, often in a
classic perihilar bat wing pattern of density. Pleural effusions also
often occur.
 CXR is important in evaluating patients with CHF for development
of pulmonary edema and evaluating response to therapy as well.
 Kerley B Lines
 These are horizontal lines less than 2cm long,
commonly found in the lower zone periphery. These
lines are the thickened, edematous interlobular
septa. Causes of Kerley B lines include; pulmonary
edema, lymphangitis carcinomatosa and malignant
lymphoma, viral and mycoplasmal pneumonia,
interstital pulmonary fibrosis, pneumoconiosis,
sarcoidosis. They can be an evanescent sign on the
CXR of a patient in and out of heart failure.
 Transthoracic echocardiography

 Transthoracic echocardiography (TTE) is the method of

choice for assessment of myocardial systolic and diastolic
function of both left and right ventricles.
 For measurement of LVEF, the modified biplane
Simpson’s rule is recommended. LV end diastolic volume
(LVEDV) and LV end systolic volume (LVESV) are
obtained from apical four- and two-chamber views.
 Doppler techniques allow the calculation of
haemodynamic variables, such as stroke volume index
and cardiac output, based on the velocity time integral at
the LV outflow tract area.
 Transoesophageal echocardiography

 Transoesophageal echocardiography (TOE) is not

needed in the routine diagnostic assessment of HF;
 however, it may be valuable in some clinical
scenarios of patients with valve disease, suspected
aortic dissection, suspected endocarditis or
congenital heart disease and for ruling out intra
cavitary thrombi in AF patients requiring
cardioversion.
 Stress echocardiography

 Exercise or pharmacological stress echocardiography

may be used for the assessment of inducible
ischaemia and/or myocardium viability and in some
clinical scenarios of patients with valve disease (e.g.
dynamic mitral regurgitation, low-flow–low-gradient
aortic stenosis).
 There are also suggestions that stress
echocardiography may allow the detection of
diastolic dysfunction related to exercise exposure in
patients with exertional dyspnoea, preserved LVEF
and inconclusive diastolic parameters at rest
 Cardiac magnetic resonance

 CMR is acknowledged as the gold standard for the measurements of volumes,

mass and EF of both the left and right ventricles. It is the best alternative
cardiac imaging modality for patients with nondiagnostic echocardiographic
studies (particularly for imaging of the right heart) and is the method of
choice in patients with complex congenital heart diseases
 CMR is the preferred imaging method to assess myocardial fibrosis using late
gadolinium enhancement (LGE) along with T1 mapping and can be useful for
establishing HF aetiology.
 CMR may also be used for the assessment of myocardial ischaemia and
viability in patients with HF and CAD (considered suitable for coronary
revascularization).
 Clinical limitations of CMR include local expertise, lower availability and
higher costs compared with echocardiography, uncertainty about safety
inpatients with metallic implants (including cardiac devices) and less reliable
measurements in patients with tachyarrhythmias. Claustrophobia is an
important limitation for CMR. Linear gadolinium based contrast agents are
contraindicated in individuals with a glomerular filtration rate (GFR) <30
mL/min/1.73m2, because they may trigger nephrogenic systemic fibrosis.
 Single-photon emission computed tomography
and radionuclide ventriculography

 Single-photon emission CT (SPECT) may be useful in

assessing ischaemia and myocardial viability.
 Gated SPECT can also yield information on
ventricular volumes and function, but exposes the
patient to ionizing radiation.
 Positron emission tomography

 Positron emission tomography (PET) (alone or with

CT) may be used to assess ischaemia and viability,
but the flow tracers (N-13 ammonia or O-15 water)
require an on-site cyclotron.
 Limited availability, radiation exposure and cost are
the main limitations.
 Coronary angiography

 Indications for coronary angiography in patients with HF are

inconcordance with the recommendations of other relevant
ESC guidelines.
 Coronary angiography is recommended in patients with HF
who suffer from angina pectoris recalcitrant to medical
therapy.
 Coronary angiography is also recommended in patients with a
history of symptomatic ventricular arrhythmia or aborted
cardiac arrest.
 Coronary angiography should be considered in patients with
HF and intermediate to high pre-test probability of CAD and
the presence of ischaemia in non-invasive stress tests in order
to establish the ischaemic aetiology and CAD severity.
Delaying or preventing the development of overt
heart failure or preventing death before the onset
of symptoms
 An inverse relationship between physical activity and the risk
of HF has been reported. A recent meta-analysis found that
doses of physical activity in excess of the guideline
recommended minimal levels may be required for more
substantial reductions in HF risk
 A primary percutaneous coronary intervention (PCI) at the
earliest phase of an ST segment elevation myocardial
infarction (STEMI) to reduce infarct size decreases the risk of
developing a substantial reduction in LVEF and subsequent
development of HFrEF.
 Initiation of an ACEI, a beta-blocker and an MRA
immediately after a myocardial infarction, especially when it
is associated with LV systolic dysfunction, reduces the rate of
hospitalization for HF and mortality, as do statins.
 Pharmacological treatment of heart failure with
reduced ejection fraction

 The goals of treatment in patients with HF are to improve their clinical status,
functional capacity and quality of life, prevent hospital admission and reduce mortality.
 ACEIs have been shown to reduce mortality and morbidity in patients with HFrEF and
are recommended unless contraindicated or not tolerated in all symptomatic patients.
ACEIs should be up-titrated to the maximum tolerated dose in order to achieve
adequate inhibition of the renin–angiotensin–aldosterone system (RAAS).
 There is consensus that beta-blockers and ACEIs are complementary, and can be
started together as soon as the diagnosis of HFrEF is made. Betablockers should be
initiated in clinically stable patients at a low dose and gradually up-titrated to the
maximum tolerated dose. Beta-blockers should be considered for rate control in
patients with HFrEF and AF, especially in those with high heart rate
 Spironolactone or eplerenone are recommended in all symptomatic patients (despite
treatment with an ACEI and a beta-blocker) with HFrEF and LVEF ≤35%, to reduce
mortality and HF hospitalization
 Loop diuretics produce a more intense and shorter diuresis than thiazides, although
they act synergistically and the combination may be used to treat resistant oedema.
However, adverse effects are more likely and these combinations should only be used
with care. The aim of diuretic therapy is to achieve and maintain euvolaemia with the
lowest achievable dose.
 Acute heart failure

 AHF refers to rapid onset or worsening of symptoms

and/or signs of HF.
 AHF may present as a first occurrence (de novo) or,
more frequently, as a consequence of acute
decompensation of chronic HF, and may be caused
by primary cardiac dysfunction or precipitated by
extrinsic factors, often in patients with chronic HF